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Adenosine Induces Cell Cycle Arrest and Apoptosis Via Cyclind1/Cdk4 and Bcl-2/Bax Pathways in Human Ovarian Cancer Cell Line Ovcar-3 Publisher Pubmed



Shirali S1 ; Aghaei M2 ; Shabani M3 ; Fathi M4 ; Sohrabi M5 ; Moeinifard M4
Authors
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Authors Affiliations
  1. 1. Department of Laboratory Sciences, Chalous Branch, Islamic Azad University, Chalous, Iran
  2. 2. Department of Clinical Biochemistry, School of Pharmacy, Isfahan University of Medical Sciences, Isfahan, P.O. Box 81746-73461, Iran
  3. 3. Department of Antibody and Antigen Engendering, Monoclonal Antibody Research Center, Academic Center for Education, Culture and Research (ACECR), Tehran, Iran
  4. 4. Department of Clinical Biochemistry, School of Medical Science, Tarbiat Modares University, Tehran, Iran
  5. 5. Department of Bacteriology, School of Medical Science, Tarbiat Modares University, Tehran, Iran

Source: Tumor Biology Published:2013


Abstract

Adenosine is a regulatory molecule with widespread physiological effects in almost every cells and acts as a potent regulator of cell growth. Adenosine has been shown to inhibit cell growth and induce apoptosis in the several cancer cells via caspase activation and Bcl-2/Bax pathway. The present study was designed to understand the mechanism underlying adenosine-induced apoptosis in the OVCAR-3 human ovarian cancer cells. MTT viability, BrdU and cell counting assays were used to study the cell proliferation effect of adenosine in presence of adenosine deaminase inhibitor and the nucleoside transporter inhibitor. Cell cycle analysis, propidium iodide and annexin V staining, caspase-3 activity assay, cyclinD1, Cdk4, Bcl-2 and Bax protein expressions were assessed to detect apoptosis. Adenosine significantly inhibited cell proliferation in a concentration-dependent manner in OVCAR-3 cell line. Adenosine induced cell cycle arrest in G0/G1 phase via Cdk4/cyclinD1-mediated pathway. Adenosine induced apoptosis, which was determined by Annexin V-FITC staining and increased sub-G1 population. Moreover, down-regulation of Bcl-2 protein expression, up-regulation of Bax protein expression and activation of caspase-3 were observed in response to adenosine treatment. The results of this study suggest that extracellular adenosine induced G1 cell cycle arrest and apoptosis in ovarian cancer cells via cyclinD1/ Cdk4 and Bcl-2/Bax pathways and caspase-3 activation. These data might suggest that adenosine could be used as an agent for the treatment of ovarian cancer. © 2013 International Society of Oncology and BioMarkers (ISOBM).
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